https://scholars.lib.ntu.edu.tw/handle/123456789/519945
標題: | Epigallocatechin gallate (EGCG) suppresses β-amyloid-induced neurotoxicity through inhibiting c-Abl/FE65 nuclear translocation and GSK3β activation | 作者: | Lin C.-L. TA-FU CHEN MING-JANG CHIU Way T.-D. Lin J.-K. |
公開日期: | 2009 | 卷: | 30 | 期: | 1 | 起(迄)頁: | 81-92 | 來源出版物: | Neurobiology of Aging | 摘要: | Alzheimer's disease (AD) is the most common neurodegenerative disease and is caused by an accumulation of Aβ plaque deposits in the brains. Evidence is increasing that green tea flavonoids can protect cells from Aβ-mediated neurotoxicity. However, the underlying mechanism remains unclear. Here, we used a human neuronal cell line MC65 conditional expression of an amyloid precursor protein fragment (APP-C99) to investigate the protection mechanism of epigallocatechin gallate (EGCG), the main constituent of green tea. We demonstrated that treatment with EGCG reduced the Aβ levels by enhancing endogenous APP nonamyloidogenic proteolytic processing. Furthermore, EGCG also decreased nuclear translocation of c-Abl and blocked APP-C99-dependent GSK3β activation, and these inhibitory effects occurred through the interruption of c-Abl/Fe65 interaction. Our results indicated that the neuroprotective action of EGCG may take place through some mechanisms other than the promotion of APP nonamyloidogenic proteolysis, as was reported previously. ? 2007 Elsevier Inc. All rights reserved. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-56049095730&doi=10.1016%2fj.neurobiolaging.2007.05.012&partnerID=40&md5=37b0557a5fd7f5a1a1bd653e5ca16940 https://scholars.lib.ntu.edu.tw/handle/123456789/519945 |
ISSN: | 0197-4580 | DOI: | 10.1016/j.neurobiolaging.2007.05.012 | SDG/關鍵字: | Abelson kinase; amyloid beta protein[1-40]; amyloid beta protein[1-42]; amyloid precursor protein; catechin; epicatechin gallate; epigallocatechin; epigallocatechin gallate; glycogen synthase kinase 3beta; protein Fe65; amyloidosis; animal experiment; animal model; article; concentration response; controlled study; enzyme activation; gene overexpression; genetic transfection; human; human cell; mouse; nerve cell; neuroblastoma cell; neuroprotection; neurotoxicity; nonhuman; priority journal; protein expression; protein interaction; protein localization; Active Transport, Cell Nucleus; Amyloid beta-Protein; Apoptosis; Catechin; Cells, Cultured; Dose-Response Relationship, Drug; Enzyme Activation; Glycogen Synthase Kinase 3; Humans; Nerve Tissue Proteins; Neurons; Nuclear Proteins; Proto-Oncogene Proteins c-abl |
顯示於: | 醫學系 |
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